Arrhythmias Flashcards
How common are arrhythmias
Pretty common
25% of pts treated with digoxin
50% of anesthetized pt
80% pts with acute MI
Do we normally treat arrhymias that are too fast or too slow?
Too fast
Tachy arrhythmia
Pros and cons of arryhmias
Can be life saving
On the other hand, there is a danger with antiarrhymic drugs in that they can paradoxically precipitate lethal arrhythmia in some patients
Where does the heart beat originate in
SA node
How does the beat travel
Goes from the SA node down the atria to the AV node
Gate keeper to the ventricles
AV
Which is worse, ventricular tachycardia or atrial tachycardia
Ventricular
What do we want to target when we treat atria?
AV node
What is the path of heart conduction
SA node, down atria, to AV node, purkinje, to ventricular
What does every step of conduction create?
AP
SA node AP
Hill
Atrial muscle AP
Steep AP
AV node AP
Hill
Perkinje AP
Steep
Ventricular muscle AP
Steep
Where do meds work for arrhythmia
On muscles and perkinje because of the steep AP
P waves
Atria gets excited
PR interval
Atrial conduction
SA node down to the AV node, span of atrial excitation
QRS interval
Ventricular being excited
Ventricular depolarization start
T wave
Ventricles repolarization
QT intervals
- ventricular depolarization to repolarization
- represents entire ventricular conduction
Fast response AP
Heart and Perkinje
Fast response in phase 0
Happen quickly, steep
What drugs do we use for fast response AP arrhymias?
Na channel blockers
K channel blockers
Na channel blockers in fast response AP arrhythmias
Depolarization causes by influx of Na, Na starts this AP and causes phase 0
-blockers with cause shift to right and less steep, means it takes longer to depolarize, slowing heart down
K channel blockers in fast response AP arrhymias
- K repolarizes membrane
- increased K inside the cell, rushing out to repolarize
- longer to repolarize with these blockers
- AP gets wider, took more time, slowed the heart down
Where is the most muscle in the heart
Ventricles
What drugs work on the ventricles
Na channel and K channel blockers
What doe Na and K channel blockers do on the ventricles
Depress ventricular depolarization
Na channel blockers affects what interval
Longer QRS interval
What interval do K channel blockers affect
Increased QT interval
What type of drugs treat ventricular arryhmias
K and Na channel blockers
Slow response AP
Gradaul and not as steep
AV and SA node
Phase IV in slow response
Spontaneous depolarization
-in ventricles it is flat.
Why is the SA node the pacemaker?
Because it is the only place in the heart with a phase IV that is as steep as it is.
-it is flat in ventricles
Where are the funny Na channels
Slow response AP
AV and SA
Phase IV
Phase 0 in slow phase
All Ca channels
What drugs do we use to treat slow response AP (SA and AV nodes)
Ca2+ channel blocker
B blockers
Ca2+ channel blockers used for slow response AP in arrhythmias
- Blocks 0 phase
- in fast response this would be Na
- depress phase IV and 0
- slow heart at SA and AV node
- if you are slowing the conduction from SA to AV, then you are slowing the atrial conduction
What drugs slows the PR interval?
Ca2+ channel blockers
B blockers in treating slow response AP for arrhythmias
- dobutamine
- if you block B receptors, you are decrease cAMP, decreasing PKA, not phosphorylation Ca2+ channels so they wont open
- indirectly blocks Ca2+
- decreased Ca2+
- depresses phase IV and 0
- good for nodes (B1 concentrated in the nodes)
What does altering calcium do to the AP?
Depresses phase IV and 0 in slow response AP
What do we use B blockers and Ca2+ channel blockers for?
Used to treat SVT (supraventricular tachycardia)
-does this by slowing the conduction between the SA and AV node, which ultimately slows atrial conduction
-
What kinds of meds are used to treat ventricular arrhymias
Na blockers
K blockers
What kind of drugs are used to treat SVT (supraventricular tachycardia/atrial)
Ca2+ blocker
B blocker
Types of SVTs
Atrial fibrillation
Paroxysmal SVT
Which is more life threatening: ventricular or atrial arrhythmias
Ventricular
What is the most common arrhythmia
Afib
Why is it important to treat SVTs even though they are not as dangerous as ventricular arrhythmia s
You need to control the AV node for SVT so that it does not make its way into the ventricles.
Types of ventricular arrhythmias
- premature ventricular complexes (PVCs)
- ventricular tachycardia
- ventricular fibrillation
Premature ventricular complexes (PVCs)
Non-life threatening. Most people experience these, can lead to ventricular tachycardia
Ventricular tachycardia
- three or more repetitive PVCs cause this
- monomorphic
- polymorphic
- leads to V fib if uncontrolled
Ventricular fibrillation
- electrical anarchy
- death ensues rapidly without tx
Monomorphic Vtach
Consistent QRS configuration
Polymorphic V-tach
Varying QRS complexes
-torsade de pointes where the QRS complexes undulate around a central axis, baseline moves all over the place
Torsades
- Type of polymorphic V tach
- QRS complex undulates around a central axis
How are the antiarrhymic drugs categorized
Class I-IV
Saved By Pharm Class
Class I antiarrhythmic drugs
- sodium channel blockers
- class 1A, 1B, and 1C
Class II antiarrhythmic drugs
-B blockers
Class III antiarrhythmic drugs
K channel blockers
Class IV antiarrhythmic drugs
Calcium channel blockers
Class IA antiarrhythmic drug
-quinidine
Class IA antiarrhythmic drug (quinidine) cardiac effects
Block Na channels and K channels; can cause widening of the QRS and QT intervals; also has antimuscarinic and a1 blocking effects to increase HR and can further cause arrhythmias
Class 1A antiarrhythmic drugs (quinidine) therapeutic use
Prevent recurring v tach
May increase mortality
Adverse effects of class 1A antiarrhythmics (quinidine)
Potential example torsades de pointes due to K channel block
- prolonged repolarization for too long, ventricles have their own intrinsic firing rate if they wait too long
- torsade is caused no K channel blockers, even though class IA is Na channel blocker, it does have some K channel blocking properties
What does blocking Na channels with a class 1A antiarrhythmic drug do
Prolongs ventricular depolariation
What does blocking of K channels with a class 1A antiarrhthymic drug do
Prolongs ventricular repolarization
What class of antiarrhymics can lead to torsades?
All class 1A Class III
Class 1B antiarrhymic drug
Lidocaine
Cardiac effects of class 1B antiarrhymic drugs (lidocaine)
Dosing channel blocker only
Therapeutic use of class 1B antiarrhymic drugs (lidocaine)
Ventricular arrhythmias
How are class 1B antiarrhythmics administered (lidocaine)
IV due to extensive first pass metabolism
When do we use class 1B antiarrhymics?
Only in acute settings
Class 1C antiarrhymic drug
Flecainaide
Cardiac actions of class Ic antiarrhymic drugs (flecainaide)
Blocks sodium
Therapeutic uses of class 1C antiaarhymic drugs
Prevent a fib, increased mortality in patients with ventricular arrhymias
When do we want to use class I drugs
Back up only
All kinda scary
What are the specific class II antiarrhythmics drugs
Atenolol and metoprolol
Class II antiarrhythmics
B blockers
- diminish phase IV and 0 depolarization
- depress automaticity at the SA node, prolong AV conduction, decrease HR
- PR interval prolonged
- good for SVTs (atrial)
What drugs are best for SVT
Class II antiarrhythmics (B blockers)
Class III antiarrhymics
Potassium channel blockers
What is the specific drugs for class III antiarrhymics
Sotalol
Amiodarone
Dronedarone
Cardiac actions of sotalol (class III antiarrthymics)
Block K channels and B receptors
- K channels for ventricular
- B receptors for SVT
Therapeutic use of sotalol (class III antiarrhymic drugs)
Ventricular arrhythmia and SVTs
Adverse effects of sotalol (class III antiarrhymics)
Bradycardia, dyspnea, fatigue (all related to B blockade); torsades (bc of K blockade)
What’s the difference between amiodarone and dronedarone
Dronedarone does not contain iodine
Actions of amiodarone/dronedarone (class III antiarrhythmics)
Amiodarone contains iodine and is related to thyroxin; both drugs similar to class I, II, III, and IV -prolongs PR, QRS, and QT
Therapeutic uses of amiodarone and dronedarone (class III antoarrhythmics)
Multipurpose
Half life of amiodarone
Several weeks
Half life of dronedarone
24 hours
Adverse effects of amiodarone and dronedarone
Pulmonary alveolitis or fibrosis, hpatotoxicity, corneal deposits, thyroid dysfunction and blue skin (amiodarone)
What drug can produce lung, liver, and eye problems?
Amiodarone and dronedarone
Which drug can cause thyroid problems and blue skin
Amiodarone
Pt is started on an antiarrhythmic drug that blocks Na, K, B, and Ca. Patient complains of bluish skin, what drug could this be
Amiodarone
Class IV antiarrhythmic
Ca2_ channel blocker
What do class IV antiarrhythmic drugs do
Decrease rate of phase IV and 0
Slowed conduction in SA, AV
What are the specific class IV antiarrhythmic drugs
Verapamil and diltiazem
-used for SVT
Can amlodipine be a good choice of CCB to use for arrhythmias?
No, we only want the ones that work on the heart. Amlodipine only works on the vessels
What are the unclassified antiarrhythmic drugs
Digoxin
Adenosine
What can digoxin be used for
Heart failure and arrhythmias
- increase contractility for HF
- slows HR by increasing vagaries firing for arrhythmias
Cardiac action of digoxin in arryhthmias
PNS effects on the atria and AV node; it can increase the PR interval due to slowing conduction in the AV node
-increased PNS activation by increased Vargas firing)
Therapeutic use of digoxin
SVT
Actions of adenosine
Naturally occurring nucleoside, decreases conduction velocity by working on adenosine receptors in the heart (Gi)
Therapeutic use of adenosine
Drug of choice for abolishing acute SVT
How must adenosine be administered
IV, acute only
Only has a duration of action of about 8s
What happens when you use adenosine on a patient
Causes them to temporarily flat line, resets the heart back to sinus rhythm
